Downregulation of IGFBP-6 or IGF-I or IGF-II expression levels via siRNAs in breast epithelial cells or knockdown IGF-1R activity on fibroblasts could play an effective role in changing fibroblast mobilization, suppressing TME remodeling and tumor invasion via the IGFs/IGF-1R axis. The gene discussed is IGF1; the disease is neoplasm.